Calcium oscillations in pancreatic acinar cells, evoked by the cholecystokinin analogue JMV-180, depend on functional inositol 1,4,5- trisphosphate receptors

Thorn, P. and Petersen, O. H. (1993) Calcium oscillations in pancreatic acinar cells, evoked by the cholecystokinin analogue JMV-180, depend on functional inositol 1,4,5- trisphosphate receptors. Journal of Biological Chemistry, 268 31: 23219-23221.


Author Thorn, P.
Petersen, O. H.
Title Calcium oscillations in pancreatic acinar cells, evoked by the cholecystokinin analogue JMV-180, depend on functional inositol 1,4,5- trisphosphate receptors
Journal name Journal of Biological Chemistry   Check publisher's open access policy
ISSN 0021-9258
1083-351X
Publication date 1993-11-05
Sub-type Article (original research)
Volume 268
Issue 31
Start page 23219
End page 23221
Total pages 3
Place of publication Bethesda, MD.
Publisher American Society for Biochemistry and Molecular Biology, Inc.
Language eng
Subject 320300 Medical Biochemistry and Clinical Chemistry
Abstract It has been reported that the synthetic heptapeptide cholecystokinin (CCK) analogue JMV-180 evokes cytosolic Ca2+ signals in pancreatic acinar cells via mechanisms that do not include either the generation or action of inositol 1,4,5-trisphosphate (InsP3) (Saluja, A. K., Dawra, R. K., Lerch, M. M., and Steer, M. L. (1992) J. Biol. Chem. 267, 11202-11207; Yule, D. I., and Williams, J. A. (1992) J. Biol. Chem. 267, 13830-13835). We have now investigated the CCK- and JMV-180-evoked cytosolic Ca2+ oscillations by measurement of the Ca(2+)-sensitive ion currents in internally perfused mouse pancreatic acinar cells. We find that the InsP3 receptor antagonist heparin (500 micrograms/ml) blocks Ca2+ oscillations induced by both CCK (5-20 pM) and JMV 180 (10-40 nM), whereas de-N-sulfated heparin (500 micrograms/ml), which does not affect InsP3 binding to its receptor, fails to inhibit the responses to the two agonists. We conclude that the cytosolic Ca2+ oscillations evoked by both CCK and JMV-180 are dependent on functional InsP3 receptors.
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Unknown

Document type: Journal Article
Sub-type: Article (original research)
Collection: School of Biomedical Sciences Publications
 
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